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Tw patho test 2

Pitting edema swelling displaced by finger depression (INTERSTITIAL EDEMA)Can signify disease
Non-pitting edema Local accumulation of edema that affects just the area of edema accumulation. (Under eye bags) long standing edema can lead to skin damage.
Causes of edema 1)increased capillary press(CHF,Clot) (2)Vasodialation(allergic rx,burns) (3)Decrease in colloid osmotic pressure(liver kidney fail) (4)lymph obstruct(filariasis, lyph removed) (5)Na/H2O excess(CHF,Hyperaldosterone, renal fail)
Inflammation A series of dynamic processes by which tissues respond to injury
Acute inflammationChronic Inflamm acute: blister, pus. chronic: Scar.
Acute inflammation Tissue events 1)Hyperemia (2) exudation (3) emigration of leukocytes
Hyperemia release of chem mediators: histamine cause vascular dialation
Histamine does two things vascular dialator and vascular damage/leakage
Effects of histamine on vasodilation vascular dialation seperates that epith cells causing gaps that leak out fluid and then proteins. Protein leakage causes decreased oncotic pressure allowing more fluid to leak out.
Acute inflammation Exudation increased release of fluid that occurs from the drop in oncotic pressure from the release of histamine. This is Edema
Types of Exudates Non cellular: (1)serous (blister) acellular; (2)fibrous contain fibrin.CELLUAR: (1)purulent: plasma,fluid,protein,bacteria(2)Suppurative: plasma,fluid,protein,bacteria and residue of tissue cells
Acute inflammation Emigration of Leukocytes Exudate enters extravascular space caused increased blood viscosity, the Hemoconcentration spreading out the bl cells (migration) and lining the epith celle (pavementing) the white blood cells start squeezing out the gaps (diapedesis)by chemotacic forces
What three things must happen for restoration of function to occur 1) Vascularization must be good (2) no perm tissue damage (3)good lymph drainage
Scar tissue Vs Granulomas tissue Scar: hard and not very vascular.Granulomas: fragile and very vascular
First intention wound healing Ex surgical incision very neat and easy to approximate ends
Secondary intention wound healing Ex Trauma with tissue loss or necrosis takes much longer to heal
Examples of Inflammatory disease 1)Coronary HD (2) ARDS (3) Asthma (4) pneumonia (5) glomerulonephritis (6) pyelonephritis (7) Inflam dis of colon (8) Cirrosis
Periodic reversible episodes of broncial spasms which impair vent. Assoc with edema of mucosa, mucus prod Asthma
Primary maifestation of asthma severe dyspnea (labored breathing) Lungs are voluminous w/out emphysema
Classifications of asthma 1) Atopic= allergic/extrinsic (2) Non-atopic=intrinsic/idioathic (3) Exercise induced (EIA) (4) Mixed
Atopic asthma characteristics 1) Mostly kids (2) assoc w/ allergies (3)diminish in later years (4) seldom assoc w/ chronic bronchitis and emphysema (5) Triggered by specific allergens * will see increase IgE
Non-atopic asthma Characteristics 1) usually adults (2) No allergy (3) Increased severity w/ age (4) assoc w/ nasal polyps, chr bronchitis, emphysema (5) TRIGGERS: non specific/ no clear reason
Non-Atopic Exercise induced asthma Charateristics 1) school aged kids (2) Attacks devel after increased activity (3) patient healthy and asymptomatic before activity
Non-Atopic MIXED asthma Charateristics 1)Adults w/ passed history of atopic or non-atopic asthma (3) accounts for the MAJORITY of cases **Can include mix of ALL asthmas
What occurs that triggers Exercise induced asthma Exer alters fluids H2O levels and increases cortisol which triggers attack. When body regulates itself attack stops.
Pathogensis of ATOPIC asthmas 1)Exposure to allergen/rx to allergen sensitivity (2) immun Rx w/IgE (3)IgE/mast cell coupling (4) Reexposure to allergen (5) Cells Release mediators: histamine, bradykinin, Leukotrienes (6) Bronch spasms (7) resp distress
In an allergic Rx what are the mast cells? Eosinophils
Why do bronchial spasms occur in asthma They are a response to allergen and bodies response to chemical mediators released (they tell the body to do this)
Pathogensis of NON-ATOPIC asthmas 1) Genetic defect in synth/metab of c-AMP (decreased avail c-AMP)(2) blockage of beta-adrenergic recep in bronchi thrfor decrease beta andrenergic stim (3) UNopposed constriction of smooth muscle(CANNOT BE STOPPED) (4) bronchial spasms (5) resp distress
Pathogensis of NON-ATOPIC asthmas made easy! The internal system has gone awry due to c-AMP defect so the system doesnt have enough to work properly, so there is no way to stop the constriction or spasms cuz homeostasis cannt stop the spasms through normal routes.
Things she finds interesting when looking at Mixed asthma DIET, obesity, poverty
Morphological Changes of asthma 1) Peribronchial smooth muscle layer-hypertrophied (constricted) (2) basement memb thickens causing collagen deposits over time (3) bronc mucosa edematous w/ inflam exudates-MAST CELLS (4) Lumen reduced diameter w/ mucus plugs causing denudation
Consequences of morph chx of asthma 1)impaired vent (2) impaired expiratory function= gas exchange (3) progressive pulmonary hyperinflation: to compensate for condstricted lumen cuz its not meeting available volume capacity
Early stage disease progression of asthma 1) Prog airway obstruc (2) prolonged expiration:dyspnea, wheezing (3) + vols trapped air (lead to pnuemothorax) (4) + residual vol (5) - IRV and vital capacity (6) Breath w/ - vol/uses + energy (7) loss of tussive force and + fatigue
LATE stage disease progression of asthma 1) Expir worsens (2)+ muscular efforts to expel air(accessory) (3) +transpulmonic press (4) Resp impairment (5) - alveolar went (6) V/Q mismatch (7) gas impar (8) cyanosis
Asthma clinical features 1) the duration of attack (2) intervals BTW attacks (3) severity (4) Status asthmaticus (5) causes of death
Status asthmaticus very severe cant move air in or out at all need EPI pen and IV steroids
Astma Treatment Prevention Avoid irritants, cold air, strenuous exerciseAnything that will trigger an attack
Astma Treatment Approaches Long term bronch inhailers, antiinflam agents, short term bronchodialators.sensitization therapy may help by exposing self to trigger agent and desensitzing.
2 functions of immune system 1) distinguish BTW self and non-self (and remove damaged self) (2) inactivate nonselfShe added...(3) immobilize the immune system response
Any agent capable of eliciting an immune response Antigen
Term for Self or natural INTRINSIC antigens Endogenous antigens: Clearing out of altered or damaged self tissues and/or cells
Term for Non-self antigen Exogenous: this turns on the immune response
Spontaneously accepted grafts autografts (self) isograft(genetically same)
Spontaneously REJECTED grafts Allografts: same species diff genotype Heterograft: Another species
Difference BTW primary response and a secondary response Primary response is slower in time and days to illicit a response and doesnt attack the antigen. Secondary takes less days to respond to reexposure, actually asttacks antigen
Immune system cells and tissues 1) skin and mucous mem (2) Phagocytes-macrophages (3) Lymph tissue (4)lympocytes (5) Null Cells
Lymph tissues include: Spleen, thymus, bone marrow, pancreas, lymph nodes
Lymphocyte- Helper T cells THelper: Thymus, CD4, secrete cytokinins: TH1: Helps other T and Macroph TH2: Help B cells w/antibody prod. (part of ADAPTIVE IMM)
Lymphocytes B-cells bone marrow, One specific Ag, ID AG makes B slpit into 1) Plasma cells: secrete Ab or Ig(2) Primed B cells: memory cells: (part of ADAPTIVE IMM)
Cytotoxic T cells CD8, Thymus, Lysis, part of adaptive immunity,recog Ag on surface and destroys w/ help from TH1. (part of ADAPTIVE IMM)
Suppressor T cells They close down the immune response after invading organisms are destroyed. **(CD8)**
Primed T cells Memory cells: part of ADAPTIVE IMM
What are the regulatory T cells? They are Helper T and Suppressor Cells, They secrete lymphkines, specifically cytokinens.(part of ADAPTIVE IMM)
Macrophages Make a "selective" attack on an Ag due to a tag IDing it as Non-self.. phagocytosis late in infect (part of ADAPTIVE IMM)
Null cells Run around killing NON-SELF: NOT SELECTIVE
Types of immunity 1)Selective: specific (marcophages) (2)Adaptive: needs 1st response, T/B cells(3) Memory: 2nd response, long term imm
IgD Not sure
IgE Histamine release, allergic Rx and paracitic infec Basophiles, mast cells
IgA Anti-infection: tears, breast milk. Primary imm in infants.shock surfaces, breast milk
IgM ABO antibodies. Stays vascular, not in tissues
IgG Most abundant/common, longest half life. Transplacental passage and NOT a good indicator of illness
cell mediated immunity T cells: target and destroy by cytolytic actioncell-cell killing
Humoral immunity B cells: target and inactivated by antibody action
Three types of immunopatho diseases 1)Hypersensitivity (2) Autoimmune diseases (3)immunodeficiencies
Hypersensitivity states Exaggerated response to common stim(EXCESSIVE)
Type 1 Hypersensitivity (B cell mediated) Need to have IgE/mast cell coupling resulting in histamine release. Local and systematic response similar to allergic Rx
Type 2 Hypersensitivity Complement activation via classical pathway, resulting in cell distruction by C9 (all lymph cells respond). Immun mediated HEMOLYTIC ANEMIA IgM/ IgG
Type 3 Hypersensitivity Classical complement act C1 by Ag/Ab resulting in vasculitis by C3-C5 releasing cytokinens C5-L5 (Neutrophils and mast cells working) Local: Arthus Rx Sys:serum sickness
Type 4 Hypersensitivity sensitized lymphocytes and macrophages (NO COMPLEMENT CYTOTOXIC T cells) its a Rx to a RxGraft rejections, dermatitis
Autoimmune diseases are systems inability to distingush BTW self and Non self (EXCESSIVE)
Pathogenesis of autoimmune diseases occur after birth, can be genetic, enviorn, mixture. Triggers are unknown. Usually assoc w/ other autoimm diseases
Classification of Autoimmune diseases 1) Organ specific: Hashimoto thyroiditis and Sympathetic ophthamia (after eyer trauma)(2) NONORGAN specific (systematic): Lupus
Immune DEFICIENCY syndromes 1) Primary: said to be genetic sex linked disorders as well as congenital (2) Secondary (aquired): due to other underlying issues ((HIV))
Primary Immune defic syndrome Ex Burton, chediak, DiGeorge, Isolated IgA, Leukocyte adhesion dis, SCID
Secondary Immune defic syndrom are aquired by: Biological: aging, stress (2) Nutritional def (3)Malignant disease (4) infections: HIV (5) Iatrogenic: radiation, chemo
HIV Theories Thought that originated from chimp to humans WEST Africa 1930's HIV 1. Then 81' first US human case HIV 2 EASTERN Africa milder
HIV characteristics Retrovirus, lentivirus: RNA-DNA (norm DNA-RNA)Viral envelope w/mem and proteins. viral core w/ RNA and RNA transcriptase inside
Viral replication steps 1) Recog BTW host cell and virus (2) att to target cells (HT/T4) (3) Inject virus into cell (4) Rev transcription RNA-DNA (5) DNA replicate (6) integration into host genome (7)act and viral replication
Integrase Enzyme that helps virus integrate into hosts cells/ genome
Consequence of HIV infection 1)+ virus cells (2) - hosts cells (3) perm infection cells w/ virus provirions (4) - of T4 = immune suppression
T4 cell count of < 200 full blown AIDS (norm 650-1200)But Tcell count used cuz cost effective, but not always reliable cuz cell counts fluctuate and asymptomatic individuals can have low count too
Types of viral load tests RT-PCR, bDNA, NASBA
Viral laods for HIV <10000 low risk, >100,000 high risk
serocoversion time for HIV 6-12 weeks
antibpody detection HIV tests Elisa: screening test:: + false +, but if - then - HIV Western blot: comfirmation test. 2 ELISA then western blot to confirm + HIV
Three reason why you would have a neg HIV testand why you test every 6 months 1) Never exposed, never infected (Ab -/Virus-) (2) tested during serumconversion window (Ab-/V+) (3) Exposed but not infected, (AB-/V-)
HAART (High Activity antiretroviral therapy) Indinavir + iamivudine(3TC) + Zidovudine(AZT)
Created by: mfish